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dc.contributor.authorDietrichs, Erik Sveberg
dc.contributor.authorMcGlynn, Karen
dc.contributor.authorAllan, Andrew
dc.contributor.authorConnolly, Adam
dc.contributor.authorBishop, Martin
dc.contributor.authorBurton, Francis
dc.contributor.authorKettlewell, Sarah
dc.contributor.authorMyles, Rachel
dc.contributor.authorTveita, Torkjel
dc.contributor.authorSmith, Godfrey L
dc.date.accessioned2020-05-15T08:20:36Z
dc.date.available2020-05-15T08:20:36Z
dc.date.issued2020-02-07
dc.description.abstract<i>Aims</i> - Treatment of arrhythmias evoked by hypothermia/rewarming remains challenging, and the underlying mechanisms are unclear. This <i>in vitro</i> experimental study assessed cardiac electrophysiology in isolated rabbit hearts at temperatures occurring in therapeutic and accidental hypothermia.<p><p> <i>Methods and results</i> - Detailed ECG, surface electrogram, and panoramic optical mapping were performed in isolated rabbit hearts cooled to moderate (31°C) and severe (17°C) hypothermia. Ventricular activation was unchanged at 31°C while action potential duration (APD) was significantly prolonged (176.9 ± 4.2 ms vs. 241.0 ± 2.9 ms, <i>P</i> < 0.05), as was ventricular repolarization. At 17°C, there were proportionally similar delays in both activation and repolarization. These changes were reflected in the QRS and QT intervals of ECG recordings. Ventricular fibrillation threshold was significantly reduced at 31°C (16.3 ± 3.1 vs. 35 ± 3.5 mA, <i>P</i> < 0.05) but increased at 17°C (64.2 ± 9.9, <i>P</i> < 0.05). At 31°C, transverse conduction was relatively unchanged by cooling compared to longitudinal conduction, but at 17°C both transverse and longitudinal conduction were proportionately reduced to a similar extent. The gap junction uncoupler heptanol had a larger relative effect on transverse than longitudinal conduction and was able to restore the transverse/longitudinal conduction ratio, returning ventricular fibrillation threshold to baseline values (16.3 ± 3.1 vs. 36.3 ± 4.3 mA, <i>P</i> < 0.05) at 31°C. Rewarming to 37°C restored the majority of the electrophysiological parameters.<p><p> <i>Conclusions</i> - Moderate hypothermia does not significantly change ventricular conduction time but prolongs repolarization and is pro-arrhythmic. Further cooling to severe hypothermia causes parallel changes in ventricular activation and repolarization, changes which are anti-arrhythmic. Therefore, relative changes in QRS and QT intervals (QR/QTc) emerge as an ECG-biomarker of pro-arrhythmic activity. Risk for ventricular fibrillation appears to be linked to the relatively low temperature sensitivity of ventricular transmural conduction, a conclusion supported by the anti-arrhythmic effect of heptanol at 31°C.en_US
dc.identifier.citationDietrichs ES, McGlynn K, Allan A, Connolly A, Bishop M, Burton F, Kettlewell S, Myles, Tveita T, Smith GL. Moderate but not severe hypothermia causes pro-arrhythmic changes in cardiac electrophysiology . Cardiovascular Research. 2019en_US
dc.identifier.cristinIDFRIDAID 1770650
dc.identifier.doihttps://doi.org/10.1093/cvr/cvz309
dc.identifier.issn0008-6363
dc.identifier.issn1755-3245
dc.identifier.urihttps://hdl.handle.net/10037/18292
dc.language.isoengen_US
dc.publisherOxford University Pressen_US
dc.relation.journalCardiovascular Research
dc.rights.accessRightsopenAccessen_US
dc.rights.holderCopyright 2020 The Author(s)en_US
dc.subjectVDP::Medisinske Fag: 700en_US
dc.titleModerate but not severe hypothermia causes pro-arrhythmic changes in cardiac electrophysiologyen_US
dc.type.versionpublishedVersionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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